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However, while hepatic and renal fibrosis could possibly be explained by the metabolic alterations present in ALMS patients, such as obesity and type 2 diabetes, it is difficult to identify a trigger insult causing fibrosis in heart, lung, bladder, testis and ovary.
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Efforts have been made to halt this spreading cortical depression using N-methyl-D-aspartate receptor antagonists and other ion channel blockers to minimize the damaging effects of CSD that can persist long after the triggering insult.
Each model has advantages and disadvantages, but these models do offer the distinct advantage of allowing the study of gut fibrosis right after the triggering insult.
It is noteworthy that the glial scar formation is associated with substantive tissue reorganization and structural changes that are long lasting and persist long after the triggering insult may have resolved.
These results suggest that antibody-mediated neurocognitive impairments may be highly specific, and that spatial cognition may be particularly vulnerable to DNRAb-mediated structural and functional injury to hippocampal cells that evolves after the triggering insult is no longer present.
As past civil-rights struggles reveal, inhumanity triggers insults, but it also deepens resolve, courage, and coalition.
Triggering insults include penetrating trauma, severe contusive trauma, invasive infections or abscess formation, neoplasm, chronic neurodegeneration, systemically triggered inflammatory challenges.
Triggering insults include penetrating trauma, severe contusive trauma, invasive infections or abscess formation, neoplasm, chronic neurodegeneration, or systemically triggered inflammatory challenges.
An excess in reactive oxygen species induced by oxidative stress directly triggers insults in the retina, including mitochondrial dysfunction, [ 40] induction of apoptosis, increased neurotoxin production, weakening of the neuroprotective functions of glial cells, and activation of immune-mediated neuronal injuries.
If true, this suggests that an intrauterine trigger or insult that is more similarly shared by MC-MZ twins may generate more comparable deficits in neural functioning that underlie the social and cognitive impairments that characterize ASD.
Chd1l might have no function at all in ES cells, its function may be masked by the function of a redundant ES cell protein, its function may only become apparent when some trigger or insult presents itself, or the ES cell protein may represent a store of protein that will be important later in development.
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